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So Chan RN TUA-SLCN
Endocrine System
The endocrine system integrates body functions by the synthesis and release of hormones The functions of the endocrine and the nervous system are interrelated. Hypothalamus: link between the nervous system and the endocrine system.
Endocrine Glands
Pituitary Gland Adrenal Glands Thyroid Glands Parathyroid Glands Gonads
Endocrine System
Endocrine Glands
secrete their products directly to the blood stream different from exocrine glands
influences metabolic activities of cells by means of hormones, which are produced by endocrine glands
y Endocrine glands: pituitary, thyroid, parathyroid,
adrenal, pineal, and thymus y The pancreas and gonads produce both hormones and exocrine products y The hypothalamus has both neural functions and releases hormones y Other tissues and organs that produce hormones: adipose cells, pockets of cells in the walls of the small intestine, stomach, kidneys, and heart
Metabolism and tissue maturation Ion regulation Water Balance Immune system regulation Heart rate and blood pressure regulation Control of blood glucose and other nutrients Control of reproductive function Uterine contractions and milk release
Hormones
Are chemical substances that are secreted by the
endocrine glands. Can travel moderate to long distances or very short distances. Acts only to cells or tissues that have receptors for the specific hormone. Target organ: the cell or tissue that responds to a particular hormone.
short duration
y Hormones leave the blood to reach target tissues or are excreted by the kidneys or liver
Regulation of Hormones
If the client is healthy, the concentration or hormones
is maintained at a constant level. When the hormone concentration rises, further production of that hormone is inhibited. When the hormone concentration falls, the rate of the production of that hormone increases.
autonomous
Hypopituitarism Hyperpituitatism
Hypopituitarism
Caused by low levels of one or more anterior pituitary
hormones.
Causes of 2 Hypopituitarism
Tumors of the hypothalamus Inflammatory disease Head injuries Surgical damage to the pituitary and/or blood vessels
Acquired Loss of body hair Infertility, decrease libido, impotence in males, amenorrhea in females
Diagnostics
X-ray, MRI or CT scan:
pituitary tumor
Plasma hormone levels:
decreased
Therapeutics
Hormonal Substitution: may be for life corticosteroids levothyroxine androgen for males estrogen for females Growth hormone
Hyperpituitarism
Hyperfunction of the anterior pituitary
gland=oversecretion of one or more of the pituitary hormones Usually caused by benign pituitary adenoma 2 most common hormones affected:
Prolactin growth hormone
Prolactinoma vs.Somatotropinoma
Prolactinoma
Female: galactorrhea menstrual disturbances,
infertility, signs of estrogen deficit (vaginal mucosal atrophy, decreased vaginal lubrication and libido)
Therapeutics
Medication bromocriptine and cabergoline (dopamine agonist) For prolactinoma and GH hypersecretion Octreotide (somatostatin) for GH hypersecretion Sx surgical remission is achieved in about 70% of patients followed over 3 years Growth hormone levels fall immediately; diaphoresis and carpal tunnel syndrome often improve within a day post-Sx Radiation Therapy for large tumors Diet
Nursing Interventions
Provide emotional support=striking body change can
cause psychological stress. Perform or assist with range of motion exercises to promote maximum joint mobility and prevent injury. Evaluate muscle weakness, especially in the patient with late stage Acromegaly. Keep the skin dry. Avoid using an oily lotion because the skin is already oily.
Nursing Interventions
Be aware that pituitary tumor cause visual problems.
If there is hemianopsia, stand where he can see you. Warn relatives that hyperpituitarism can cause inexplicable mood changes. If the patient is a child, explain to the parents that surgery prevents permanent soft-tissue deformities but won t correct bone changes that have already occurred. After an operation, emphasize the importance of continuing hormone replacement therapy.
Transphenoidal Hypophysectomy
Endoscopic, transnasal,
transsphenoidal pituitary microsurgery. Removal of adenoma while preserving anterior pituitary function in most patients. Surgery is usually well tolerated, but complication occur in about 10%.
Postoperative care
WOF: Bleeding operative site is patched with muscle or fat-> sutures easily disrupted. keep the patient on bed rest for 24 hours after surgery and encourage ambulation thereafter keep the head of bed elevated (30) to avoid placing tension or pressure on the suture line. Instruct the patient not to sneeze, cough, blow his nose, or bend over for several days to avoid disturbing the suture line. Arrange for visual field testing as soon as possible because visual defects can indicate hemorrhage.
Postoperative Care
WOF: CSF leak and infection reinforce measures to prevent increased ICP oral care, BUT the patient should not brush his teeth for 2 weeks to avoid suture line disruption Signs of CSF leak Frequent clearing of the throat and swallowing Presence of halo ring on gauze Test for glucose Signs of infection Fever, headache, nuchal rigidity
Postoperative Care
WOF: Post-Op pain Mild analgesics for headache caused by CSF loss during surgery or paranasal pain.
Paranasal pain typically subsides when the catheters
Postoperative Care
WOF: Diabetes Insipidus
due to inadequate release of ADH usually happens 24 to 48 hours after surgery and may resolve within 72 hours. be alert for increased thirst and increased specific gravity. Management I & O, urine sp. Gravity and daily weight monitoring Fluid replacement Aqueous vasopressin, sublingual desmopressin acetate.
Postoperative Care
WOF: S/Sx of hypopituitarism
patient may need hormonal replacement therapy due to decreased pituitary secretion of tropic hormones. Necessary: cortisol immediate post-op Maintenance hormonal replacement as needed
o o o o Cortisol Thyroxine Estrogen or Testosterone Vasopressin
metabolism
Released during stress or
in response to an increase plasma osmolality to stimulate reabsorption of water and decreased urine output.
Diabetes Insipidus
Disorder characterized by massive polyuria due to
Diabetes Insipidus
Central Diabetes Insipidus: Deficiency of vasopressin Primary diabetes Insipidus ( without an identifiable organic lesion noted on MRI of the pituitary and hypothalamus)
May be familial, occurring as a dominant trait, or ( idiopathic ) Due to damage to the hypothalamus or pituitary stalk by tumor, anoxic encephalopathy, surgical or accidental trauma, infection (encephalitis, tuberculosis, syphilis), sarcoidosis, or multifocal langerhans cell (eosinophilic) granulomatosis ( histiocytosis X )
Diabetes Insipidus
Diabetes Insipidus
Signs and Symptoms Polyuria-> enormous daily output of very dilute urine, waterlike urine with specific gravity of 1.001 to 1.005 Intense thirst (patient tends to drink 4 to 40liters of fluid daily), especially with a craving for ice water, Dehydration-> weight loss, poor tissue turgor, dry mucous membranes, constipation, muscle weakness, dizziness. Inadequate water replacement results in Hyperosmolality (irritability, mental dullness, coma, hyperthermia) because of dehydration and hypernatremia Hypovolemia (hypotension, tachycardia and shock eventually)
Diabetes Insipidus
Diagnostics Fluid deprivation test-> to differentiate between psychogenic polydipsia and DI Administration of desmopressin->to differentiate between central DI and nephrogenic DI 24 hour urine collection of volume, glucose, and creatinine Serum for glucose, urea nitrogen, calcium, uric acid, potassium and sodium.
Therapeutics
y Medications For central DI
For nephrogenic DI: Indomethacin-hydrochlorthiazide (with potassium supplementation) Indomethacin-demopressin Indomethacin-amiloride Clofibrate, chlorpropamide and thiazide diuretics (mild DI) Psychotherapy
persistent excretion of
concentrated urine signs of fluid overload change in level of consciousness NO EDEMA HYPONATREMIA
Causes of SIADH
Tumors: bronchogenic carcinoma, lymphoma,
pancreatic cancer, mesothelioma Pulmonary: TB, pneumonia, lung abscess, COPD, pneumothorax, HIV secretion CNS: meningitis, head injury, subdural hematoma, subarachnoid hemorrhage, neurosurgery Drugs: some medications (vincristine, phenotiazines, tricylic antidepressants, thiazide diuretics, and others) and nicotine have been implicated in SIADH; they either directly stimulate the pituitary gland or increase the sensitivity of renal tubules to circulating ADH.
mosmol/kg) High urine sodium excretion (>20 mmol/L) Normal renal function (low BUN<10mg/dL),absence of hypothyroidism and glucocorticoid deficiency and recent diuretic therapy.
SIADH: Management
Maintain fluid balance Restriction or water intake (<1,000ml/day). (takes 3-10 days to work) If the patient has evidence of fluid overloading, a history of CHF, or is resistant to treatment, loop diuretics (furosemide) may be added as well. Chronic treatment: lithium or demeclocycline which inhibit ADH action. Monitoring of body weight.
SIADH: Management
Maintain sodium balance Increase sodium intake if the serum sodium is below 120 or if the patient is seizing, emergency treatment: 3% NaCL. May be followed by furosemide. Excessively rapid correction of hyponatemia may cause central pontine myelinolysis. Patients with a plasma sodium concentration greater then 125 mmol/L rarely need specific therapy for hyponatremia.
of gluconeogenesis. Increase protein catabolism Increasing mobilization of fatty acids promote Na and H2O retention Anti-inflammatory effect Aid the body in coping with stress
aldosterone system
Adrenal Medulla
Release catecholamines Epinephrine Norepinephrine Released during fight or flight situations->
SYMPATHETIC effect
Cushing s Syndrome
Complications
Osteoporosis Peptic Ulcer Immune and inflammatory response is also
compromised
Other complications include HPN, and sexual and
psychological complications
ACTH dependent. 24-hour urine collection for cortisol, midnight serum cortisol Dexamethasone suppression test-> 1mg dexamethasone given at 11 pm and serum cortisol taken at 8am the next day.
Cortisol level <5ug/dl excludes Cushing s syndrome with
98% certainty
Protect client from exposure to infection, monitor WBC Maintain skin integrity Minimize stress Provide diet low in calories, sodium and high in protein, potassium, calcium and vitamin D Monitor for urine glucose and acetone, administer insulin if necessary Prepare client for adrenalectomy if needed
Hyperaldosteronism
y Hypersecretion of aldosterone from the adrenal cortex y Two types: Primary disease of the adrenal cortex Secondary condition due to increased plasma renin activity y Causes: Excessive reabsorption of sodium and water Excessive renal excretion of potassium
Hyperaldosteronism: Causes
y Primary hyperaldosteronism: Autonomous secretion of aldosterone from the adrenals Benign adrenal adenoma (Conn s syndrome) y Secondary hyperaldosteronism: High renin state-> stimulating aldosterone release Renal artery stenosis Wilm s tumor Pregnancy Oral Contraceptive use Nephritic syndrome Cirrhosis with ascites Heart failure
Hypokalemia
Muscle weakness and fatigue Paresthesia and Arrhytmias Polyuria and Polydipsia Tetany from alkalosis
Hypernatremia
Hyperaldosteronism: Diagnostics
Hypokalemia Hypernatremia Elevated serum bicarbonate and pH Hypomagnesemia Elevated plasma and urinary aldosterone Decreased Renin in 1 hyperaldosteronism Increased Renin in 2 hyperaldosteronism Low specific gravity urine (diluted urine)
Hyperaldosteronism: Treatment
y Primary hyperaldosteronism: Unilateral adrenalectomy
Potassium-sparing diuretic (such as spironolactone or amiloride)-> may lead to decreased libido, gynecomastia, impotence Antihypertensives Aminogluthetimide-> inhibits synthesis of aldosterone. Diet: sodium restriction, increased potassium Treatment of secondary hyperaldosteronism: include correction of the underlying cause.
Adrenal Insufficiency
1 adrenal insufficiency: Addison s disease The most common form of adrenal hypofunction-> occurs when more than 90% of the adrenal gland is destroyed Autoimmune process-> decreased secretion of androgen, glucocorticoids, and mineralocorticoids. 2 adrenal Insufficiency: It may also be caused by a disorder outside the gland Aldosterone secretion frequently continues. Nursing Alert! Adrenal crisis (addisonian crisis) is a medical emergency requiring immediate, vigorous treatment.
Adrenal Insufficiency:causes
y Autoimmune destruction of the adrenal gland,
tuberculosis, bilateral adrenalectomy, hemorrhage into the adrenal gland, neoplasms, or fungal infections.
y Secondary adrenal hypofunction is caused by Hypopituitarism Abrupt withdrawal of long term corticosteroid therapy In a patient with adrenal hypofunction, adrenal crisis
occurs when the body s stores of glucocorticoids are exhausted by trauma, infection, surgery, or other physiologic stressors.
hand creases and over the metacarpophalangeal joints, elbows, and knees. y Poor coordination y Fasting hypoglycemia; and craving for salty food. y Amenorrhea y Adrenal crisis
Profound weakness and fatigue, shock, severe nausea
increased-> hyperpigmentation
Adrenal Insufficiency
Decreased plasma cortisol levels and serum sodium
levels.
BUN level.
5 L of IV fluids, dextrose
periodically because steroid replacement may necessitate changing the insulin dosage.
Pheochromocytoma
Rare disorder, a chromaffin-cell tumor of the
sympathetic nervous system, usually in the adrenal medulla, secretes an excess of the catecholamines epinephrine and norepinephrine.
This causes episodes of hypotension and symptoms of
catecholamine excess.
The tumor is usually benign but may be malignant in
Pheochromocytoma
feelings of impending doom, abdominal or chest pain, tachypnea, N&V, fatigue, wt. loss, constipation, postural hypotension, paradoxical response to antiHPNs(common), hyperglycemia
Pheochromocytoma:
y Diagnostic tests: Increased plasma levels of catecholamines, elevated blood sugar, glucosuria
Elevated urinary catecholamines and urinary VMA
Nursing considerations! Avoid coffee, nuts, chocolate, banana, vanilla. Tumor on CT scan.
Pheochromocytoma: Treatment
Surgical removal of the tumor with sparing of the
Anti-hypertensives: Alpha-adrenergic blocker ( phentolamine, prazosin, or phenoxybenzamines) A beta-blocker (propanolol) Metyrosine may be used to block catecholamine
synthesis.
Adrenalectomy
y Resection or removal of one or both adrenal glands. y The treatment of choice For adrenal hyperfunction and hyperaldosteronism Adrenal tumors, such as adenomas and pheochromocytomas.
Adrenalectomy: Pre-op
y Correct electrolyte imbalance Potassium, sodium, calcium Manage hypertension
common because handling of the adrenal glands stimulates catecholamine release. y WOF: adrenal crisis-> hypotension, hyponatremia, hyperkalemia y Remember, glucocorticoids from the adrenal cortex are essential to life and must be replaced to prevent adrenal crisis until the hypothalamic, pituitary, and adrenal axis resumes functioning.
directed.
y If patient had unilateral adrenalectomy, explain that
Hyperthyroidism Hypothyroidsim
connected by an isthmus y The gland is about 5cm long and 3cm wide and weighs about 30g y It produces 3 hormones: T3, T4, and calcitonin
Biopsy
Sampling Thyroid
Tissue to: detect malignancy Initial test for evaluation of thyroid masses.
Plummer s nails
Hyperthyroidism
y Or thyrotoxicosis y Increased metabolic rate y Causes: o Grave s disease o Initial manifestations of thyroiditis (hashimoto s and subacute thyroiditis) o Toxic adenoma o TSH-secreting pituitary tumor o Factitious thyrotoxicosis o Jodbasedow disease o Amiodarone-induced
Enlarged thyroid gland Tachycardia-> atrial fibrillation, heart failure Hypertension Heat intolerance, diaphoresis Smooth, soft, warm skin Fine Soft Hair Diarrhea, weight loss inspite of increased appetite Nervousness and fine tremors of hands. Hyperactive reflexes, body weakness Personality changes, mood swings Osteoporosis Clubbing and swelling of fingers, Plummer s nails Menstrual disturbances, decreased fertility
loss, diplopia
y Pretibial Edema
Hyperthyroidism
Thyroid Storm
y A medical emergency: high mortality y Marked delirium, severe tachycardia, vomiting, diarrhea,
Hyperthyroidism: Diagnostics
y Radioimmunoassay test shows elevated T4 and T3. y Thyroid scan reveals increased radioactive iodine
(123I) uptake. y TSH in 1 hyperthyroidism y TSH in 2 hyperthyroidism y Orbital sonography and CT scan confirm subclinical ophthalmopathy
Hyperthyroidism: Management
y Propylthiouracil (PTU) and methimazole y Used for pregnant women and patient who refuse
surgery or 131I treatment. y During pregnancy PTU, is the preferred therapy y A few (1%) of the infants born to mothers receiving antithyroid medication will be hypothyroid. y Mechanism of action
Blocks thyroid hormone synthesis
WOF: Agranulocytosis
Hyperthyroidism: Management
y Radioactive iodine (131I), potassium or sodium
iodide (Potassium iodide SSKI), strong iodine solution (Lugol s solution) y Adjunct with other antithyroid drugs in preparation for thyroidectomy y Treatment for thyrotoxic crisis:
Inhibits the release and synthesis of thyroid hormones Decreases the vascularity of the thyroid gland Decreases thyroidal uptake of radioactive iodine
y y y y
SSKI) strong iodine solution (Lugol s solution) Category D Dilute oral doses in water or fruit juice and give with meals to prevent gastric irritation, to hydrate the patient, and to mask the very salty taste Warn the patient that sudden withdrawal may precipitate thyrotoxicosis Store in a light-resistant container Give iodides through a straw to avoid tooth discoloration Force fluids to prevent fluid volume deficit
overnight before administration After dose for hyperthyroidism, the patient s urine and saliva are slightly radioactive for 24 hours; vomitus is highly radioactive for 6 to8 hours. Institute full radiation precautions during this time Instruct the patient to use appropriate disposal methods when coughing and expectorating.
for 24 to 48 hours so amount of radioactive material excreted can be determined Or flush the toilet twice after urination
48 hours after drug administration to facilitate excretion. Limit contact with the patient to 30 minutes per shift per person the 1st day; may increase time to 1 hour on 2nd day and longer on the 3rd day.
Hyperthyroidism
B- blockers, Digoxin, anticoagulation Prednisone for opthalmopathy Treatment for thyroid storm: o PTU o I.V. propanolol to block sympathetic effects o Corticosteroids to replace depleted cortisol levels o Iodide to block release of thyroid hormone
Hyperthyroidism: Management
Surgery: Thyroidectomy For exopthalmos Suggest sunglasses or eye patches to protect his eyes from light Moisten the conjunctivae often with artificial tears Warn the patient with severe lid retraction to avoid sudden physical movement that might cause the lid to slip behind the eyeball. Elevate the head of bed to reduce periorbital edema Stress the importance of regular medical follow-up after discharge because hypothyroidism may develop from 2 to 4 weeks pot-op Drug therapy and 131I therapy require careful monitoring and comprehensive teaching
Hypothyroidism
A state of low serum thyroid hormone levels or cellular resistance
to thyroid hormone Causes May result from thyroidectomy Radiation therapy Chronic autoimmune thyroiditis ( Hashimoto s Thyroiditis) Inflammatory conditions such as amyloidosis and sarcoidosis Pituitary failure to produce TSH Hypothalamic failure to produce thyrotropin-releasing hormone(TRH) Inborn errors of thyroid hormone synthesis An inability to synthesize thyroid hormone because of iodine deficiency. Use of antithyroid medications such as PTU.
Hypothyroidism
Weakness Fatigue Forgetfulness Cold intolerance Unexplained weight gain Constipation Goiter Slow speech Decreasing mental stability
inelastic skin.
Hypothyroidism
y Puffy face, hands and feet y Dry, sparse hair y Thick, brittle nails y Slow pulse rate y Anorexia y Abdominal distention y Menorrhagia y Decreased libido y Infertility y Ataxia y Intentional tremor
Myxedema Coma
Manifests as hypotension, bradycardia, hypothermia,
hyponatremia, hypoglycemia, respiratory failure, coma Can be precipitated by acute illness, rapid withdrawal of thyroid medication, anesthesia, surgery, hypothermia, use of opioids
Hypothyroidism : Diagnostics
Radioimmunoassay tests: T3 & T4
TSH level with 1 hypothyroidism TSH in 2 hypothyroidism Serum cholesterol and triglyceride levels are increased
Management
Prevention: Prophylactic iodine supplements to decrease the incidence of iodine deficient goiter Symptomatic cases: Hormonal replacement: synthroid
(synthetic hormone (levothyroxine)) -dosage is increased q 2-3weeks
doctor if with
Chest pain, palpitations, sweating, nervousness, or other
same time each day to maintain constant hormone levels. Suggest a morning dosage to prevent insomnia
Monitor apical pulse and BP. If pulse is >100bpm,
of thyroid medication even if his symptoms subside: Maintain patent airway Administer meds-synthroid, glucose, corticosteroids. IV fluid replacement Wrap patient in blanket Treat infection or any underlying illness
Hyperparathyroidism
y Characterized by excess
activity or one more of the four parathyroid glands, resulting in excessive secretion of parathyroid hormone(PTH) y Maybe primary or secondary
Hyperparathyroidism: causes
y 1 hyperparathyroidism: Single adenoma, genetic disorders, or MEN 2 hyperparathyroidism: Rickets, vitamin D deficiency, chronic renal failure, phenytoin or laxative abuse.
Hyperparathyroidism
y Effect of PTH secretion: Calcium Through increased bone resorption, increased GI and renal absorption of calcium Complications Renal calculi-> renal failure Osteoporosis Pancreatitis Peptic ulcer
Hyperparathyroidism
THINK OF HYPERCALCEMIA: CNS: psychomotor and personality disturbances, loss of memory for recent event, depression, overt psychosis, stupor and possibly, coma.
GI: anorexia, N&V dyspepsia, and constipation. Neuromuscular: fatigue; marked muscle weakness and
insufficiency
Skeletal and articular: chronic lower back pain and
subcutaneous calcification.
Hyperparathyroidism: Dx
serum PTH levels serum Ca and decreased Phosphorus levels. X-rays may show diffuse demineralization of bones Elevated alkaline phosphatase
Hyperparathyroidism: Treatment
Surgery to remove the adenoma Force fluids; limiting dietary calcium intake For life threatening hypercalcemia: promote sodium
and calcium excretion, using normal saline solution (up to 6L in life-threatening situations), furosemide, and administering oral sodium or potassium phosphate, Calcitonin Postmenopausal women: estrogen supplements
Hypoparathyroidism
A deficiency of PTH PTH primarily regulates calcium
balance; hypoparathyroidism leads to hypocalcemia and produces neuromuscular symptoms ranging from paresthesia to tetany.
Hypoparathyroidism
Congenital absence or malfunction of the parathyroid glands. Autoimmune destruction Removal of or injury to one or more parathyroid glands during
neck surgery Rarely, from massive thyroid radiation therapy. Ischemic infarction of the parathyroids during Sx. Diseases, such as amyloidosis or neoplasms Suppression of normal gland function caused by hypercalcemia(reversible) Hypomagnesemia-induced impairment of hormone secretion(reversible)
easily.
Hypoparathyroidism
Decreased PTH and serum calcium levels Elevated serum phosphorus levels X-rays reveal increased bone density ECG: prolonged Qti, QRS-complex ST-elevation
changes.
Diabetes Mellitus
Stimulating active transport of glucose into muscle and adipose tissue Promoting the conversion of glucose to glycogen for storage Promoting conversion of fatty acids into fat Stimulating protein synthesis
Secreted in response to high blood sugar Found in cells of the islets of langerhans
Secreted in response to low blood sugar Found in the -cells of the islets of langerhans
Diabetes Mellitus
Chronic disease characterized by hyperglycemia It is due to total or partial insulin deficiency or insensitivity of the cells to insulin Characterized by disorders in the metabolism of CHO, FAT and CHON as well changes in the structure and function of blood vessels.
Types of DM
Type 1 or IDDM
Usually occurs in children or in non-obese adults Usually occurs in obese adult over age 40
Induced by trauma, surgery, pancreatic disease or medications Can be treated as either type 1 or type 2
Type 2
y Gradual y Mostly in adults y Frequently obese y Rare y Absent y Can be normal, decreased, or
(typically young) Body Habitus- Usually thin Ketosis- common Autoantibodies-present in most cases Endogenous insulin- low or absent
increased.
PathophysiologyHyperglycemia
Lack of insulin causes
polyphagia
Cont. pathophysiology
y The body turns to fats
and protein for energy; but in the absence of glucose in the cell, fats cannot be completely metabolized and ketones are produced
Chronic Complications
Microangiopathy:
retinopathy, nephropathy Macroangiopathy: peripheral vascular disease: peripheral vascular disease, atheroscelrosis, CAD Neuropathy
ESRD
Diabetic Foot
Wash feet daily with mild soap and lukewarm water. Dry thoroughly between toes by pressure. DO NOT RUB vigorously, as this is apt to break the delicate skin Rub well with vegetable oil to keep them soft, prevent excess friction, remove scales, and prevent dryness. If the feet become too soft and tender, rub them with alcohol about once a week.
toes. If varicose veins are present, massage the feet very gently; never massage the legs. If the toenails are brittle and dry, soften them by soaking for 1 hr each night in lukewarm water containing 1 tsbp of powdered sodium borate (borax) per quart. Clean around nails become too long, file them with an emery board. File them straight across and no shorter than the underlying soft tissue of the toes. Never cut the corner of the nails.
feet correctly. The shoes should have wide toes that will cause no pressure, fit close in the arch, and grip the heels snugly. Wear new shoes one-half hour on the first day and increase by 1 hour each day following. Wear thick, warm, loose stockings. Treatment of Corns and Calluses Corns and calluses are due to friction and pressure, most often from improperly fitted shoes and stockings. Wear shoes that fit properly and cause no friction or pressure.
lukewarm (not hot) water, using a mild soap, for about 10 minutes and then rub off the excess tissue with a towel or file. Do not tear it off. Under no circumstances must the skin become irritated. Do not cut corns or calluses. If they need attention it is safer to see a podiatrist. Prevent callus formation under the ball of the foot (a) by exercise, such as curling and stretching the toes several times a day; (b) by finishing each step on the toes and not on the ball of the foot. And (c) by wearing shoes that are not too short and that do not have high heels
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Therapeutic interventions
y Lifestyle changes
- Weight control and exercise - Planned diet
g
g g
50-60% of calories are complex carbohydrates, high fiber 12-20% of daily calories is protein, 60-85g/day Fat intake not to exceed 30% of daily calories, more of polyunsaturated/ monounsaturated fats Basic tools: food exchange groups Self monitoring of blood glucose Moderation in alcohol intake Using artificial sweetener is acceptable
Insulin Ultra rapid acting insulin analog (humalog) Short acting insulin (Human regular insulin) Intermediate acting insulin (Humulin lente, Humulin NPH) Long acting Insulin (Protamine zinc, humulin ultralente) Premixed insulin (70% NPH, 30% regular)
Peak 1 hour
Duration 3 hours
4-6 hours
3-4 hours
4-12 hours
16-20 hours
6-8 hours
12-16 hours
20-30 hours
30min-1 hour
2-12 hours
18-24 hours
Insulin Dose
y 2 units y 4 units y 6 units y 8 units y 10 units y Refer to MROD, EFOD or
Diabetology Fellow.
resistance
y Dawn Phenomenon - increase in blood sugar because
insulin
Somogyi Phenomenon
Rebound Hyperglycemia at early morning
Hypoglycemia at dawn
Decrease dose of IAI at 10 PM
acting simple carbohydrate (glucose tablets, fruit juice, and soda) If unconscious, glucagon SQ or IM If in the hospital, 25-5o cc of D5050 (50% dextrose in 50cc vial)
Oral Hypoglycemics
o Sulfonyureas Promotes increase insulin secretion from pancreatic beta cells through the stimulation( requires at least 30% normally functioning beta cells) 1st gen-agents:
2nd gen-agents:
Oral Hypoglycemics
y Biguanides Reduces hepatic production of glucose by inhibiting glucogenolysis Decrease the intestinal absorption of glucose and improves lipid profile Agents
Oral Hypoglycemics
Thiazolidinediones-enhances action at the cell and
ketones in the body causing metabolic acidosis o Occurs in insulin dependent Diabetic client o Precipitating factors: Undiagnosed DM, neglect of treatment, infection, other physical or emotional stress o Onset slow, maybe hours to days
Emergency Management
y For both DKA and HHNK, treat dehydration first with
300mg/dl WOF too rapid correction, it can cause rapid fluid shifts (brain edema and increased ICP, ARDS) IV regular insulin 0.1 unit/kg bolus then 0.1 u/kg/hr drip Correcting electrolyte imbalance. WOF hypoK as a result of treatment. For severe acidosis (pH <7.1), DKA patients may have to be given NaHCO3
DKA
HHNK
Hyperglycemia Hyperosmolarity Polyuria (osmotic diuresis) Dehydration DM type II Elderly Patients on TPN, burn
Hyperglycemia (>600mg/dl) Hyperosmolarity(>320 mOsm/L) pH >7.3 (no acidosis)
S/sx
Type of patients
Lab Findings
Mortality rate
10% to 20%
Always strive for excellence in everything that you do. Thank You Very Much DCSC RN